Cuffed endotracheal and tracheostomy tubes are invaluable for maintaining ventilation in the management of the critically-ill patients. These tubes are sealed in the tracheal or bronchial lumen by inflating a balloon-like cuff which surrounds the airway tube. The cuff permits maintenance of airway pressures during mechanical inflation of the lungs by the respirator, and also prevents aspiration of the regurgitated gastro-esophageal contents. However, a hazard caused by the use of the device is the damage inflicted to the tracheal or bronchial wall by the inflated cuff.
The most common complications include loss of mucosal cilia, ulceration, hemorrhage, tracheal or bronchial stenosis, tracheoesophageal fistula and tracheal dilation. All of these complications are considered to result from the pressure exerted against the tracheal or bronchial mucosa by the inflated cuff, resulting in impaired local perfusion and ischemia of the site under the cuff. Currently there is no established method of bedside evaluation of this mucosal injury except intermittent endoscopic examination of the cuff site. However, this is an invasive procedure, and there could be inter- and intra-observer variations. This may not detect the early injury which could be reversible by simple management, such as simply decreasing the intra-cuff pressure by removing small amount of air from the cuff.
Also this procedure may require transient deflation of the cuff to visualize the area under the cuff, which could cause aspiration of gastric regurgitant.
To overcome these problems, it is essential to review the pathophysiology of tracheal injury at the cuff site. It is generally accepted that the nature of tracheal injury is ischemic, resulting from low perfusion by cuff pressure. Thus, to monitor the injury of the tracheal wall at the cuff site, it is reasonable to follow the degree of ischemia at the inflicted tracheal wall. For better understanding of the pathophysiology of tissue ischemia of hypoperfusion, it is essential to review the acid-base buffer system of cells.
In normal physiologic condition, there is carbonic acid/bicarbonate buffer system in equilibrium with hydrogen ion as in equation I. EQU H.sup.+ +HCO.sub.3.sup.- .rarw..fwdarw.H.sub.2 CO.sub.3 .rarw..fwdarw.H.sub.2 O+CO.sub.2 (I)
When hydrogen ion is increased by any cellular metabolism or insults, the reaction will proceed toward the right in equation I. Then it will result in decreased level of bicarbonate, increased production of carbon dioxide to buffer the increase of hydrogen ion level. Finally, the elevation of carbon dioxide will be lowered by rapid diffusion of carbon dioxide across the cell membrane to venous blood, where it will be transfered to central ventilation system. In tissue hypoxia of low perfusion, intracellular hydrogen ion level is increased by anaerobic metabolism or hydrolysis of ATP. Also, because of low perfusion, carbon dioxide will not be lowered well enough. As a result, intracellular hydrogen ion level will remained high without being buffered well enough, futher causing metabolic derangement.
Let's assume that in the equilibrium state of normal perfusion, hydrogen is Al(nEq/L), bicarbonate level Bl(mEq/L), carbonic acid level Cl(m mol/L), partial pressure of carbon dioxide Dl(mm Hg), and the volume of the solution is Q(Liter). Here, let's suppose that certain amount (p m mol) of hydrogen ion is added and carbon dioxide is not going to be cleared out of the system as in tissue hypoperfusion. If the concentration of hydrogen ion, bicarbonate, carbonic acid, and partial pressure of carbon dioxide is A2,B2,C2 and D2 respectively, then EQU (C2)*Q=(C1)*Q+P (II)
Since the solubility coefficient for carbon dioxide is 0.0301 m mol/L/mm Hg, EQU C1=(0.0301)*D1 (III) EQU C2=(0.0301)*D2 (IV)
The following can be easily derived from equation II, III and IV. EQU P/Q=(0.0301)*(D2-D1) (V)
It has been well known that tissue ischemia secondary to low perfusion is characterized by increased production of hydrogen ion, carbon dioxide in the cells and insufficient transfer of the carbon dioxide out of the component cells. Therefore it is reasonable to follow the hydrogen ion and carbon dioxide levels to monitor the degree of the ischemia of a tissue. That is, the extent of hydrogen ion level added in the cell can represent the degree of insults caused by hypoperfusion.
By equation (V), the amount of added hydrogen ion can be estimated by monitoring the carbon dioxide level in normal(Dl) and hypoperfusion(D2) state. Since carbon dioxide diffuses freely, intracellular carbon dioxide level in normal cells is considered equal to that of arterial blood. Free gas can penetrate silicone membrane easily, but not liquid. Thus, carbon dioxide level in the under-perfused cells can be estimated by implanting a silicone membrane chamber into the target tissue. The chamber is then perfused with saline that equilibrates to the average carbon dioxide of the surrounding tissue medium.
The measurement of carbon dioxide of tissue has been tried in soft tissue, bone, and gastrointestinal tract. In gastrointestinal tonometry, Fiddian-Green introduced the concept of tonometric pHi, which was derived by Henderson-Hasselbalch equation. However, arterial bicarbonate was used for calculation instead of intracellular level. Therefore it is not clear at present what the pHi indicates clinically, even though there are several reports that it correlates well to intracellular pH measured directly. In one animal experiment, the pHi does not correlate well especially when actual wall pH of the intestine becomes lower ranges(underperfused state). Therefore, apparently it is more physiologic to follow arterial and tonometrically-derived carbon dioxide level rather than ambiguously-defined pHi.
Accordingly, this invention is directed to provide an instrument and a method for monitoring the degree of tracheal wall injury caused by the inflated cuff pressure during mechanical ventilation.